The purpose of this research is to specify further the anatomical characteristics of the brain in developmental dyslexia. Three brains have been examined in our lab, and all have shown anatomical anomalies that can be traced to the fetal period. Although all 3 brains shared in common the presence of neuronal ectopias and architectonic dysplasias, the locaton and severity of these lesions are variable. Additional brains will be examined in an attempt to correlate the severity and location of the anatomical findings to dyslexic syndromes. A search will also be made for additional pathologies, "negative cases", and developmental anomalies in unaffected family members and unrelated controls. Brains have been and will continue to be received through a brain bank established with the Orton Dyslexia Society. The specimens will be processed in whole-brain celloidin-embedded serial sections stained for cell bodies, myelinated fibers and additional strains as needed to interpret the pathological findings. Attention will be paid to anomalies of developmental origin and to cytoarchitectonic structure and asymmetry. The second, and related, portion of the grant will aim at characterizing the cortical anomalies that have been discovered in the brains of autoimmune New Zealand mice. The relevance for further study in this animal is that: 1) immune-related disorders have been shown to be increased in frequency among left-handers and learning disabled individuals and their families; and 2) the cortical anomalies in the New Zealand mice bear a strong resemblance to the anomalies described in the dyslexics. The major effort in this portion of this study will be to specify the architectonic and histological characteristics of the abnormalities in this animal, and to relate these to age, sex, laterality, and, preliminarily, to behavior. The results will be used in future experiments aimed at disclosing intrauterine influences in the formation of brain anomalies. The New Zealand mouse may then become a powerful animal model for the study of anatomical mechanisms in dyslexia.